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Sex is expensive. For example, the daughters of an asexual female can reproduce at twice the rate of the progeny descended from a sexual female, assuming a sex ratio of one male to one female. So why is sex maintained despite this apparent disadvantage? One suggestion has been that the lack of meiotic recombination in asexual lineages results in the accumulation of mutations in a sexuals. Paland and Lynch (p. 990; see the Perspective by Nielsen) studied sexual and obligate asexual lineages of Daphnia (water fleas). Through a process of selective interference, the asexual lineages developed a fourfold greater number of mildly deleterious mutations in their mitochondrial genomes compared to the sexual lineages.

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does it mean mutations that result in measurably reduced fitness? under what conditions?

It’s not clear from the abstract whether they actually measured just how deleterious the mutations are, as opposed to just the frequency increase of the mutations.

It’s more curiosity, as obviously an ever increasing mutation load in mito DNA would have the end result of decreasing the overal fitness of the individuals posessing them, but it would be good to know exactly how far this was tested.

moreover, while I’m not conversant with the biology of Daphnia, and I know that in some species, recombination of MtDNA does occur (see for example http://www.lifesci.sussex.ac.uk/CSE/members/mladoukakis/pdfs/rokas.TREE03.pdf ), Ron does raise an interesting point.

Could you point to the relevant references that indicate why the authors chose to study the mutation rates in the MtDNA instead of the primary genome in this species? I’m sure I’m missing something.

for another perspective on the evolution and maintenance of asexuality/sexuality in Daphnia, check this paper out:

Daphnia is not an exception, the mitochondria do not recombine.
From the paper…”The predicted acceleration in mutational decay in asexual lineages extends to the normally nonrecombining mitochondrial genes because the loss of segregation between nuclear and organelle genomes, analogous to the loss of recombination between nuclear loci, subjects such genes to selective interference from the entire nuclear genome.”

Earlier in the paper they explain that meiosis is suppressed in the asexual lineages. I think they are saying that since meiosis isn’t happening the entire genome, including the organelle genome, is one big linkage group. So the mitochondrial genome behaves like a nuclear gene in terms of accumulating mutations.

Sir Toejam-
Usually “mildly deleterious mutations” refers to those causing a 1-5% decrease in fitness (the cutoff varies depending on the researcher).

They measured the fitness effect of the mutations as a ratio between synonymous (Ks) and nonsynonymous (Ka) amino acid substitutions (so they sequenced 13 mitochondrial genes and counted substitutions). If mutations were neutral then Ka = Ks. If mutations are deleterious then Ka will be less than Ks. If the mutations are beneficial Ka will exceed Ks.

They then used differences in Ka/Ks across a phylogeny to estimate the percentage of mutations of different effects… I’m not sure I quite get how they did this yet… So they didn’t directly measure the effects of mutations, they used an indirect but commonly employed method.

As for the use of mitochondria, in the paper they state that mitochondria have a higher mutation rate and this gives them more power to detect an effect.

not having studied molecular genetics for about 20 years now, can I reasonably assume that the reason for looking at the mutation rates in mtDNA would simply be that it’s much easier to sequence and amplify the relevant bits?

As for the use of mitochondria, in the paper they state that mitochondria have a higher mutation rate and this gives them more power to detect an effect.

ah, you posted before i finished writing my response.

thanks again.

this is kinda why i hate asking these questions without direct access to the whole paper, but then i probably wouldn’t have bothered even asking if I did, and perhaps there are others who got something out of it.

I’m sorry, Dr. Flank. How was I to know that one dirty comment was going to open the floodgates for people to post porn links? (Could someone disemvowel that post? If I should ever desire porn, I do not need help from the Panda’s Thumb getting it.) Besides, while my post wasn’t keeping with the discussion, it was related to the original topic - that sexual reproduction is better than asexual at preventing accumulation of nasty mutations. And it was kind of funny, right? Right? Anyone?

Speaking of, (I noticed that these comments ended where they belong - on the bathroom wall) what was that post about? was it spam? was it a joke? That’s the first time I’ve ever seen something like that on PT.

…”The predicted acceleration in mutational decay in asexual lineages extends to the normally nonrecombining mitochondrial genes because the loss of segregation between nuclear and organelle genomes, analogous to the loss of recombination between nuclear loci, subjects such genes to selective interference from the entire nuclear genome.”

This quote makes no sense to me. I happen to know alot about this subject, been thinking about it and have written one paper on the topic. The ‘loss of segregation between nuclear and mitochondrial’ part is incomprehensible.

My first reaction to the reported result is that, if true, it would be quite interesting but there is no obviously simple explanation for why it should work this way. I think the authors do not realize that yet. (But then perhaps I should read the whole paper before criticizing one poorly worded paragraph)

…”The predicted acceleration in mutational decay in asexual lineages extends to the normally nonrecombining mitochondrial genes because the loss of segregation between nuclear and organelle genomes, analogous to the loss of recombination between nuclear loci, subjects such genes to selective interference from the entire nuclear genome.”

This quote makes no sense to me. I happen to know alot about this subject, been thinking about it and have written one paper on the topic. The ‘loss of segregation between nuclear and mitochondrial’ part is incomprehensible.

My first reaction to the reported result is that, if true, it would be quite interesting but there is no obviously simple explanation for why it should work this way. I think the authors do not realize that yet. (But then perhaps I should read the whole paper before criticizing one poorly worded paragraph)

mike-
The whole paper is written rather poorly, similar to that paragraph. I am struggling as well with the meaning of that quote, as well as with some other stuff they discuss. This is my field too (I’m a grad student) and Lynch usually does pretty good stuff but this paper is NOT well-written.

There is some supplementary material that I haven’t checked out yet, maybe that will answer some questions.